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This Article Full Text Full Text (PDF) All Versions of this Article: 295/2/H610    most recent 00107.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Ashikaga, H. Articles by Covell, J. W. PubMed PubMed Citation Articles by Ashikaga, H. Articles by Covell, J. W.

Changes in regional myocardial volume during the cardiac cycle: implications for transmural blood flow and cardiac structure

Department of Medicine and Bioengineering, University of California, San Diego, La Jolla, California

Submitted 1 February 2008 ; accepted in final form 27 May 2008

Although previous studies report a reduction in myocardial volume during systole, myocardial volume changes during the cardiac cycle have not been quantitatively analyzed with high spatiotemporal resolution. We studied the time course of myocardial volume in the anterior mid-left ventricular (LV) wall of normal canine heart in vivo (n = 14) during atrial or LV pacing using transmurally implanted markers and biplane cineradiography (8 ms/frame). During atrial pacing, there was a significant transmural gradient in maximum volume decrease (4.1, 6.8, and 10.3% at subepi, midwall, and subendo layer, respectively, P = 0.002). The rate of myocardial volume increase during diastole was 4.7 ± 5.8, 6.8 ± 6.1, and 10.8 ± 7.7 ml·min^–1·g^–1, respectively, which is substantially larger than the average myocardial blood flow in the literature measured by the microsphere method (0.7–1.3 ml·min^–1·g^–1). In the early activated region during LV pacing, myocardial volume began to decrease before the LV pressure upstroke. We conclude that the volume change is greater than would be estimated from the known average transmural blood flow. This implies the existence of blood-filled spaces within the myocardium, which could communicate with the ventricular lumen. Our data in the early activated region also suggest that myocardial volume change is caused not by the intramyocardial tissue pressure but by direct impingement of the contracting myocytes on the microvasculature.

myocardial structure; ventricular pacing; mechanical dyssynchrony